Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Neuza DominguesMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal. neuza.domingues@uc.pt.ORCID 0000-0002-2073-412X
Alessia Calcagni'Telethon Institute of Genetics and Medicine (TIGEM), Naples, Italy.ORCID 0000-0002-1946-5815
Sofia FreireMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.ORCID 0009-0002-2316-1096
Joana PiresMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.
Ricardo CasqueiroMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-8808-9756
Ivan L SalazarMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-9667-6766
Niculin Joachim HerzDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Tuong HuynhDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0002-5595-419X
Katarzyna WieciorekUniversity Medical Center Göttingen, Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, Göttingen, Germany.
Tiago Fleming OuteiroUniversity Medical Center Göttingen, Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, Göttingen, Germany.ORCID 0000-0003-1679-1727
Henrique GirãoCoimbra Institute for Clinical and Biomedical Research (iCBR), Centre for Innovative Biomedicine and Biotechnology, Academic and Clinical Center of Coimbra, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-5786-8447
Ira MilosevicMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-6440-3763
Andrea BallabioTelethon Institute of Genetics and Medicine (TIGEM), Naples, Italy.ORCID 0000-0003-1381-4604
Nuno RaimundoMultidisciplinary Institute of Ageing, Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal. nuno.raimundo@psu.edu.ORCID 0000-0002-5988-9129
Funding
Dissecting and targeting lysosomal signaling in kidney tumorigenesisR01CA260205 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI ANDREA BALLABIO, Roberto Zoncu · 2022 to 2026
$2.7M
Associazione Italiana per la Ricerca sul Cancro A.I.R.C IG-22103Deutsche Forschungsgemeinschaft (DFG) SFB1190-P02EC | Horizon 2020 Framework Programme (H2020) 857524European Research Council Advanced H2023 AdG; INCANTAR 101097752Fondazione Telethon (FT) 337327HHS | National Institutes of Health (NIH) R01-CA260205MEC | Fundação para a Ciência e a Tecnologia (FCT) 2022.09311.PTDCNCI NIH HHS R01 CA260205Wellcome TrustWellcome Trust (WT) 224361/Z/21/Z
6 · The paper itself
Abstract
Batten disease is characterized by early-onset blindness, juvenile dementia and death within the second decade of life. The most common genetic cause are mutations in CLN3, encoding a lysosomal protein. Currently, no therapies targeting disease progression are available, largely because its molecular mechanisms remain poorly understood. To understand how CLN3 loss affects cellular signaling, we generated human CLN3 knock-out cells (CLN3-KO) and performed RNA-seq analysis. Our multi-dimensional analysis reveals the transcriptional regulator YAP1 as a key factor in remodeling the transcriptome in CLN3-KO cells. YAP1-mediated pro-apoptotic signaling is also increased as a consequence of CLN3 functional loss in retinal pigment epithelia cells, and in the hippocampus and thalamus of Cln3
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Loss of the lysosomal protein CLN3 triggers c-Abl-dependent YAP1 pro-apoptotic signaling. · full record | OpenQuestion